Abstract

Cognitive fatigue and autonomic abnormalities are frequent symptoms in MS. Our model of MS-related fatigue assumes a shared neural network for cognitive fatigue and autonomic failures, i.e., aberrant vagus nerve activity induced by inflammatory processes. Therefore, they should occur in common. To explore the relationship between cognitive fatigue and autonomic symptoms in MS patients, using self-reported questionnaires. In 95 MS patients, cognitive fatigue was assessed with the Fatigue Scale for Motor and Cognitive Functions and autonomic abnormalities with the Composite Autonomic Symptom Scale-31 (COMPASS-31). We used exploratory correlational analyses and hierarchical regression analysis, controlling for age, depressive mood, disease status, and disease duration, to analyze the relation between autonomic abnormalities and cognitive fatigue. The cognitive fatigue score strongly correlated with the COMPASS-31 score (r = 0.47, p < 0.001). Regression analysis revealed that a model, including the COMPASS-31 domains: pupillomotor, orthostatic intolerance, and bladder, best predict the level of cognitive fatigue (R2 = 0.47, p < 0.001) after forcing the covariates into the model. In MS patients, cognitive fatigue and autonomic dysfunction share a proportion of variance. This supports our model assuming that fatigue might be explained at least partially by inflammation-induced vagus nerve activity.

Highlights

  • Fatigue and autonomic abnormalities, such as cardiovascular or bladder dysfunctions, are frequent symptoms in multiple sclerosis decreasing a patient’s quality of life

  • We checked for differences between the rr MS, sp MS, and pp MS patients in the cognitive score of the Fatigue Scale for Motor and Cognitive Functions (FSMC) and the scales of the COMPASS-31 using one-way ANOVA and Kruskal–Wallis H test, respectively

  • We found no significant difference between groups for the cognitive Fatigue Scale of the FSMC, the COMPASS-31 total score, and its subscores apart from the gastrointestinal subscore [χ2(2) = 7.86, p = 0.020] and the bladder subscore [χ2(2) = 11.85, p = 0.003]

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Summary

Introduction

Fatigue and autonomic abnormalities, such as cardiovascular or bladder dysfunctions, are frequent symptoms in multiple sclerosis decreasing a patient’s quality of life. Hanken et al [6] developed a model for explaining fatigue in MS patients According to this model, increased bodily inflammation plays a major role in the generation of MS-related fatigue. It assumes that proinflammatory cytokines activate the afferents of the vagus nerve which convey information about bodily inflammation to interoceptive brain areas, such as the nucleus tractus solitarius, the hypothalamus, the insular cortex, the anterior cingulate cortex, and the amygdala. Our model of MS-related fatigue assumes a shared neural network for cognitive fatigue and autonomic failures, i.e., aberrant vagus nerve activity induced by inflammatory processes.

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